Evidence for abnormal calcium homeostasis in patients with adynamic bone disease

Abstract

To investigate whether the derangements in calcium kinetics in patients with renal osteodystrophy are similar in the various histologic forms of this metabolic bone disease, 43 patients on chronic maintenance dialysis underwent calcium kinetic studies using the double isotope technique, iliac crest bone biopsies for mineralized bone histology and histomorphometry and determinations of serum indices of calcium and bone metabolism. Intestinal calcium absorption was not different among the three histologic groups. However, women exhibited lower calcium absorption in each histologic form (P < 0.01). Patients with predominant hyperparathyroid bone disease showed plasma calcium efflux, calcium accretion rate and calcium retention markedly above normal values. Patients with low turnover bone disease exhibited a normal or slightly decreased plasma calcium efflux and calcium accretion rate together with a disproportionately low calcium retention. Patients with mixed uremic osteodystrophy presented with a calcium kinetic profile intermediary to the two other forms. Good relationships existed between plasma calcium efflux, calcium accretion rate, calcium retention and histomorphometric parameters of bone turnover as well as serum levels of parathyroid hormone. However, no serum parameter could indicate with certainty the underlying bone disease. These findings demonstrate that adynamic bone disease does not merely represent an academic finding but is characterized by a very low bone capacity to buffer calcium and inability to handle an extra calcium load. This is particularly relevant for the daily care of end-stage renal failure patients presently receiving higher than ever amounts of vitamin D and calcium salts.

Calcium Metabolism in the Early Posttransplantation Period

“…Our data are in accordance with previous Ca kinetic studies of maintenance dialysis patients that showed a significant and direct relationship between serum PTH levels and plasma Ca efflux (24).…”

Renal osteodystrophy in the first decade of the new millennium: Analysis of 630 bone biopsies in black and white patients

“…Low bone turnover is not merely a histologic entity; it also has important clinical ramifications. Patients with low bone turnover have abnormal calcium homeostasis, (12) and it was shown that low bone turnover is associated with vascular calcifications. (27) The study also shows that white patients are more likely to present with low bone turnover than blacks.…”

“…The abnormalities encompass changes in bone turnover (T), mineralization (M), bone balance and the result of it, which is bone volume (V). Clinically, disorders in bone turnover (T) are associated with disturbed mineral homeostasis (12,13) and increased fracture risk. (14) Defective mineralization (M) may result in bone pain and/or fracture.…”

Npt2b Deletion Attenuates Hyperphosphatemia Associated with CKD

“…[28][29][30] Evidence derived from classic clinical radiolabel studies suggests that the inability of bone to serve as a buffer for excess calcium and phosphate contributes to serum phosphate elevations and may lead to deposition of excess mineral in soft tissues. 31,32 We therefore determined the effect of Npt2b deletion on bone disease in the adenine mouse model. Classic features of high turnover, including increased bone formation rates, elevated mineral apposition rates, and increased osteoid surface, were observed in uremic mice as an apparent consequence of elevated PTH (Figure 6).…”